黄连素对水银神经毒性的神经保护作用
汞（Hg）是公知的具有神经毒性的重金属。大量研究表明，Hg的神经毒性与谷氨酸介导的兴奋性毒性之间有密切联系。汞的神经毒性与（氧/氮）水平的增加簇的反应相关联。此外，增加的细胞内钙水平容易激活一氧化氮合酶，作为NMDA谷氨酸受体的过度活化的结果，增加一氧化氮的形成。再次，细胞内钙水平增加可触发钙依赖性损害性过程，导致细胞成分的不可逆的损害，并最终导致细胞死亡。
小檗科植物的根部和树皮中提取的小檗碱具有抗炎、抗氧化的作用，并具有较好的血脑屏障通透性，因此，埃及阿勒旺大学Ahmed E. Abdel Moneim教授实验室研究了小檗碱对的Hg神经毒性的神经保护作用。此观点发表在《中国神经再生研究（英文版）》杂志2015年第6期上。
Article: "Mercury-induced neurotoxicity and neuroprotective effects of berberine" by Ahmed E. Abdel Moneim (Department of Zoology and Entomology, Faculty of Science, Helwan University, Cairo, Egypt)
Abdel Moneim AE (2015) Mercury-induced neurotoxicity and neuroprotective effects of berberine. Neural Regen Res 10(6):881-882.
欲获更多资讯：
文章全文请见：http://www.nrronline.org/
Mercury-induced neurotoxicity and neuroprotective effects of berberine
Mercury (Hg) is a heavy metal of known toxicity, it naturally occurs in several physical and chemical forms: elemental or metallic mercury (Hg0), inorganic mercury [(mercurous (Hg+) and mercuric
(Hg2+)] and organic mercury (in which mercury is bonded to methyl, ethyl, phenyl, or similar groups), and all of it can produce toxic effects even in low doses. As a result of the involvement of oxidative stress and apoptosis in mercury-induced neurotoxicity, Ahmed E. Abdel Moneim’s laboratory has been investigating the neuroprotective role of berberine. Berberine (BN) is one of protoberberine isoquinoline alkaloid extracted from the roots and barks of many plants of the Berberis species. Due to its high blood brain barrier permeability, the beneficial neuroprotective effect of BN in Hg exposure was studied. Hg-induced neurotoxicity was partially elucidated. In this regard, glutamate and calcium dyshomeostasis, as well as ROS generation, are three important and interrelated phenomena that mediate a toxic cycle that culminates in neuronal death. Whereas, BN possesses neuroprotective effects via antioxidant defense stimulation. BN also decreased oxygen consumption and increased mitochondrial membrane potential, which improved mitochondrial function, leading to protection
against oxidative stress. In addition, BN attenuated Hg-induced apoptotic neuronal cell death by increasing anti-apoptotic signaling (Bcl-2), and decreasing apoptotic signaling (Bax, cytochrome c and caspase). This perspective article is published in Neural Regeneration Research (2015, Vol. 10, No. 6)
Article: "Mercury-induced neurotoxicity and neuroprotective effects of berberine" by Ahmed E. Abdel Moneim (Department of Zoology and Entomology, Faculty of Science, Helwan University, Cairo, Egypt)
Abdel Moneim AE (2015) Mercury-induced neurotoxicity and neuroprotective effects of berberine. Neural Regen Res 10(6):881-882.
黄连素对水银神经毒性的神经保护作用
汞（Hg）是公知的具有神经毒性的重金属。大量研究表明，Hg的神经毒性与谷氨酸介导的兴奋性毒性之间有密切联系。汞的神经毒性与（氧/氮）水平的增加簇的反应相关联。此外，增加的细胞内钙水平容易激活一氧化氮合酶，作为NMDA谷氨酸受体的过度活化的结果，增加一氧化氮的形成。再次，细胞内钙水平增加可触发钙依赖性损害性过程，导致细胞成分的不可逆的损害，并最终导致细胞死亡。
小檗科植物的根部和树皮中提取的小檗碱具有抗炎、抗氧化的作用，并具有较好的血脑屏障通透性，因此，埃及阿勒旺大学Ahmed E. Abdel Moneim教授实验室研究了小檗碱对的Hg神经毒性的神经保护作用。此观点发表在《中国神经再生研究（英文版）》杂志2015年第6期上。
Article: "Mercury-induced neurotoxicity and neuroprotective effects of berberine" by Ahmed E. Abdel Moneim (Department of Zoology and Entomology, Faculty of Science, Helwan University, Cairo, Egypt)
Abdel Moneim AE (2015) Mercury-induced neurotoxicity and neuroprotective effects of berberine. Neural Regen Res 10(6):881-882.
欲获更多资讯：
文章全文请见：http://www.nrronline.org/
Mercury-induced neurotoxicity and neuroprotective effects of berberine
Mercury (Hg) is a heavy metal of known toxicity, it naturally occurs in several physical and chemical forms: elemental or metallic mercury (Hg0), inorganic mercury [(mercurous (Hg+) and mercuric
(Hg2+)] and organic mercury (in which mercury is bonded to methyl, ethyl, phenyl, or similar groups), and all of it can produce toxic effects even in low doses. As a result of the involvement of oxidative stress and apoptosis in mercury-induced neurotoxicity, Ahmed E. Abdel Moneim’s laboratory has been investigating the neuroprotective role of berberine. Berberine (BN) is one of protoberberine isoquinoline alkaloid extracted from the roots and barks of many plants of the Berberis species. Due to its high blood brain barrier permeability, the beneficial neuroprotective effect of BN in Hg exposure was studied. Hg-induced neurotoxicity was partially elucidated. In this regard, glutamate and calcium dyshomeostasis, as well as ROS generation, are three important and interrelated phenomena that mediate a toxic cycle that culminates in neuronal death. Whereas, BN possesses neuroprotective effects via antioxidant defense stimulation. BN also decreased oxygen consumption and increased mitochondrial membrane potential, which improved mitochondrial function, leading to protection
against oxidative stress. In addition, BN attenuated Hg-induced apoptotic neuronal cell death by increasing anti-apoptotic signaling (Bcl-2), and decreasing apoptotic signaling (Bax, cytochrome c and caspase). This perspective article is published in Neural Regeneration Research (2015, Vol. 10, No. 6)
Article: "Mercury-induced neurotoxicity and neuroprotective effects of berberine" by Ahmed E. Abdel Moneim (Department of Zoology and Entomology, Faculty of Science, Helwan University, Cairo, Egypt)
Abdel Moneim AE (2015) Mercury-induced neurotoxicity and neuroprotective effects of berberine. Neural Regen Res 10(6):881-882.